Bacterial etiology and antibiotic resistance profile of bloodstream infections in human immunodeficiency virus patients from Southern India.

Sir,

Human immunodeficiency virus (HIV) patients continue to be at high risk of acquiring bacterial bloodstream infections (BSIs) despite antiretroviral treatment.[1] Clinical utility of high-class antibiotics, especially the third-generation cephalosporins and carbapenems as treatment options, drives the emergence of multidrug-resistant (MDR) bacteria.[2] Studying bacterial etiology of BSI in HIV patients and understanding their resistance rate to antibiotics would help in the proper antibiotic selection for treatment regimens and avoid further emergence of antibiotic resistance. Reports on BSI and its antimicrobial resistance profile in HIV patients from southern India remain scarce. Hence, this study aimed to retrospectively analyze (2009–2017) the bacterial etiology of BSI in HIV patients attending YRG CARE, Chennai, using conventional culture techniques, and from 2017, BSI was identified using BD BACTEC™ FX 40 automated blood culture system (Becton, Dickinson and Company, USA). Antibiotic-resistant profile was determined using Kirby–Bauer disc diffusion method as per the CLSI guidelines.[3]

A total of 51 (5.24%) bacterial strains were isolated from blood specimens collected from 972 HIV patients. Staphylococcus aureus caused high level of BSI (47), followed by Escherichia coli (33.3%), Klebsiella pneumoniae (6%), Salmonella spp. (4%), Pseudomonas aeruginosa (2%), and Enterococcus spp. (2%). High positivity of BSI was observed in the year 2014 (n = 15; 29.4%) followed by 2016 (n = 10; 19.6%). Positivity of BSI was higher among male (74.5%; n = 38) than female (25.5%; n = 13) HIV patients. BSI was highly seen in patients within the age group of 31–45 years (mean age: 40.3 years). Hospitalized HIV patients showed higher rate of (n = 38; 74.5%) BSI. S. aureus strains from BSI were highly resistant to ofloxacin (75%), penicillin (71%), azithromycin (58.3%), erythromycin (54.2%), and methicillin/oxacillin (50%). E. coli exhibited high level of resistance to ampicillin (82.3%) followed by ceftazidime (82.3%), cefotaxime and ciprofloxacin (76.5%), and cefazolin, ceftriaxone, cefuroxime, levofloxacin, meropenem, and piperacillin (57.1%). A steep increase in resistance was observed among E. coli strains against amoxiclav (14.3%–57.1%), cefepime (14.3%–57.1%), and cefazolin, cefuroxime, and ceftriaxone (from 25% to 50%) from 2009 to 2017. K. pneumoniae isolates exhibited 100% resistance against ampicillin and ceftazidime, followed by 66.7% to cefotaxime, ciprofloxacin, and meropenem [Table 1].

Table 1

Year-wise antibiotic resistance profile of Staphylococcus aureus and Escherichia coli isolated from bloodstream infections in human immunodeficiency virus patients

Class of antibiotics	Antibiotics	Study periods
		2009	2010	2011	2012	2013	2014	2015	2016	2017
Staphylococcus aureus
Fluoroquinolones	Ciprofloxacin	0	0	0	0	9.1	18.2	9.1	45.5	9.1
	Levofloxacin	0	0	0	0	0	0	16.7	66.7	16.7
	Ofloxacin	11.1	5.5	0	0	5.5	22.2	16.6	27.	5.5
Lincosamides	Clindamycin	0	0	0	0	16.7	33.3	16.7	16.7	16.7
Tetracyclines	Doxycycline	0	0	0	0	33.3	0	0	33.3	0
Macrolides	Azithromycin	0	0	0	0	7.1	21.4	28.6	28.6	7.1
	Erythromycin	0	0	0	0	7.7	31	23.1	23.1	7.7
Aminoglycosides	Gentamicin	0	11.1	0	0	11.1	33.3	11.1	22.2	0
Antistaphylococcal β-lactams	Oxacillin	25	8.3	0	0	0	8.3	16.6	25	8.3
Penicillin	Penicillin	0	0	0	0	5.9	29.4	29.4	23.5	5.9
Ansamycins	Rifampicin	33.3	0	0	0	0	11.1	11.1	33.3	11.1
Escherichia coli
Aminoglycosides	Amikacin	0	0	0	0	0	50	50	0	0
	Gentamicin	0	0	0	11.1	0	44.4	11.1	11.1	22.2
Penicillins + β-lactamase inhibitor	Amoxyclav	0	0	0	-	0	-	14.3	28.8	57.1
Penicillins	Ampicillin	0	0	0	7.1	0	35.7	14.3	14.3	28.6
Nonextended spectrum cephalosporins; 1st and 2nd generation cephalosporins	Cefazolin	0	0	0	-	0	-	25	25	50
	Cefuroxime	0	0	0	-	0	-	25	25	50
Extended-spectrum cephalosporins; 3rd and 4th generation cephalosporins	Cefepime	0	0	0	-	0	-	14.3	28.8	57.1
	Ceftazidime	0	0	0	7.1	0	35.7	14.3	14.3	28.6
	Cephotoxime	0	0	0	7.7	0	38.5	15.4	15.4	23.1
	Ceftriaxone	0	0	0	-	0	-	25	25	50
Cephamycins	Cefoxitin	0	0	0	-	0	-	40	40	20
Fluoroquinolones	Ciprofloxacin	0	0	0	7.7	0	31	15.4	15.4	31
	Levofloxacin	0	0	0	0	0	-	25	25	50
Folate pathway inhibitors	Co-trimoxazole	0	0	0	14.3	0	-	28.8	14.3	42.8
Carbapenems	Imipenem	0	0	0	0	0	0	50	0	50
	Meropenem	0	0	0	0	0	12.5	25	25	37.5
Antipseudomonal penicillins + β-lactamase inhibitors	Piperacillin	0	0	0	-	0	-	25	25	50
	Piperacillin-tazobactam	0	0	0	-	0	-	66.6	0	33.3
Tetracyclines	Tetracycline	0	0	0	-	0	-	33.3	33.3	33.3

Immune dysregulation among HIV patients results in increased risk of morbidity due to S. aureus causing BSI.[1] Gram-negative bacteria were reported to be responsible for one-fifth of all BSIs, among which E. coli and P. aeruginosa were reported more frequently.[4] Contrarily, here, Gram-positive bacteria (S. aureus; 47%) caused high level of BSI than Gram-negative bacteria (E. coli; 33.3%). From Malawi,[5] a 19-year surveillance study reported that E. coli, S. aureus, and Klebsiella spp. caused 8.8%, 6.6%, and 4.4% of BSI in non-HIV patients, respectively. In this current study, E. coli exhibited extended resistance profile to carbapenem antibiotics (39.6%), especially against imipenem (50%), which is contrasting to the other study where E. coli isolated from HIV patients had shown 100% sensitivity to imipenem.[6] Increased level of antibiotic resistance makes difficult the treatment of BSI caused by carbapenem-resistant Enterobacteriaceae and also by aminoglycoside and fluoroquinolone resistant bacteria. This study concludes that methicillin-resistant S. aureus (MRSA) and the third-generation cephalosporin- and carbapenem-resistant Enterobacteriaceae were the main etiological agents responsible for BSI in HIV patients. Incidence of MRSA and MDR Enterobacteriaceae increases the severity of BSI due to its resistance profile, making clinical management and antibiotic selection highly challenging in our resource-limited HIV care setting.

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Conflicts of interest

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